ArticleLeukemia research and treatment2012
Pathogenesis of Metastatic Calcification and Acute Pancreatitis in Adult T-Cell Leukemia under Hypercalcemic State.
Article in Leukemia research and treatment, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 17 citations in OpenAlex.
- Calcinosis Cutis Presenting as Multiple Discharging Sinuses in Skin: A Case Report.JNMA; journal of the Nepal Medical Association · 2025Article
- The Intricate Process of Calcification in Granuloma Formation and the Complications FollowingBiomolecules · 2025Review
- Vascular Calcification: Molecular Networking, Pathological Implications and Translational Opportunities.Biomolecules · 2024Review
- Generalized Arterial Calcification of Infancy (GACI): Optimizing Care with a Multidisciplinary Approach.Journal of multidisciplinary healthcare · 2022Review
- An Iranian Woman with Parathyroid Adenoma and Palpable Breast Masses Due to Bilateral and Asymmetric Calcifications.Indian journal of surgical oncology · 2020Article
- Hypercalcemic crisis due to adult T cell leukemia: a rare cause of paralytic ileus.Annals of gastroenterology · 2012Article
- A DRAMATIC RESPONSE TO DENOSUMAB: PROTRACTED HYPOCALCEMIA RELATED TO HUMAN T-CELL LYMPHOTROPIC VIRUS TYPE 1-ASSOCIATED ADULT T-CELL LEUKEMIA/LYMPHOMA.AACE clinical case reportsArticle
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human T-cell leukemia virus type-1 (HTLV-1) is the causative agent of adult T-cell leukemia (ATL). Hypercalcemia is common in patients with ATL. These patients rarely develop metastatic calcification and acute pancreatitis. The underlying pathogenesis of this condition is osteoclast hyperactivity with associated overproduction of parathyroid hormone-related protein, which results in hypercalcemia in association with bone demineralization. The discovery of the osteoclast differentiation factor receptor activator of nuclear factor-κB ligand (RANKL), its receptor RANK, and its decoy receptor osteoprotegerin (OPG), enhanced our understanding of the mechanisms of ATL-associated hypercalcemia. Macrophage inflammatory protein-1-α, tumor necrosis factor-α, interleukin-1, and interleukin-6 are important molecules that enhance the migration and differentiation of osteoclasts and the associated enhanced production of RANKL for osteoblast formation. In this paper, we focus on metastatic calcification and acute pancreatitis in ATL, highlighting recent advances in the understanding of the molecular role of the RANKL/RANK/OPG system including its interaction with various cytokines and calciotropic hormones in the regulation of osteoclastogenesis for bone resorption in hypercalcemic ATL patients.
Identifiers
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.